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Biomedical subjects

T Hano

Publications and source records attributed to T Hano.

At least 73 records · Page 4Linked to original sources
PubMed1989

Blood pressure and sympathetic activity following responses to aerobic exercise in patients with essential hypertension.

Fourteen untreated patients with essential hypertension (EH) were subjected to mild aerobic exercise with the intensity at 50% of the maximum oxygen uptake (VO2max) twice a week for 12 weeks, as compared with 14 normotensive subjects (NT). Blood pressure and norepinephrine (NE) in plasma, platelet and urine were measured as the indices of sympathetic activity. In EH, a significant fall in both systolic and diastolic blood pressure was observed. In addition, exercise training produced a significant decrease both urinary and platelet NE, but not in plasma NE. Neither significant changes in blood pressure nor NE in plasma, platelet and urine were observed in NT. These results suggest that an inhibition of the sympathetic nervous system might be related to the blood pressure fall in physical exercise training.

Adult↗
PubMed1989

[Contribution of calmodulin to renin release in spontaneously hypertensive rats].

A comparative study was designed to evaluate the contribution of calmodulin to renin release from isolated glomeruli of spontaneously hypertensive rats (SHR, Okamoto and Aoki). Male 7-week-old SHR and age-matched control Wistar-Kyoto rat (WKY) were used in the present study. Glomeruli were isolated by the method of Beierwaltes et al. Isolated glomeruli were placed within the superfusion chamber and perfused with Krebs-Ringer solution at a constant flow of 0.3 ml/minute at 37 degrees C. Renin release was increased by calmodulin inhibitor, W-7 in both SHR and WKY. SHR showed higher maximal levels of renin release by W-7 compared to WKY. This result indicates that calmodulin plays an inhibitory role in renin release from juxtaglomerular cells. Calmodulin-mediated suppression mechanism in renin release is augmented in SHR.

Animals↗
PubMed1988

Relationship between the sympathetic nervous system and sodium potassium adenosine triphosphatase inhibitor in salt-sensitive patients with essential hypertension.

In order to evaluate endogenous Na+,K+-ATPase inhibitor on sympathetic nerve endings, endogenous Na+,K+-ATPase inhibitor and plasma noradrenaline were determined in patients with essential hypertension under different sodium conditions. Compared with the plasma from non-salt-sensitive patients, that from salt-sensitive patients showed significantly higher Na+,K+-ATPase inhibitor and plasma noradrenaline levels. Salt-induced changes in endogenous Na+,K+-ATPase inhibitor and those in blood pressure or plasma noradrenaline showed positive correlations. These results suggest that the salt-induced increase in endogenous Na+,K+-ATPase inhibitor might induce blood pressure elevation in essential hypertension, at least partly via increased noradrenaline levels.

Blood Pressure↗
PubMed1988

Contributions of the sympathetic nervous system, vasopressin and baroreceptor function in brain angiotensin II excess-induced hypertension in the dog.

To determine the principal effects of brain angiotensin(Ang) II on the sympathetic nervous system, vasopressin (AVP), and the high and low pressure baroreceptor systems, we observed the hemodynamic and neurohumoral characteristics induced by the acute(1-hr) and chronic(1-wk) infusion of Ang II into the brain ventricle in conscious dogs, and then evaluated the hemodynamic responses to sole-innervated carotid artery occlusion(COR) after Ang II infusion and again after vagotomy in anesthetized dogs. Both acute(50ng/kg/min) and chronic(15ng/kg/min) infusion of Ang II caused a significant rise in arterial pressure without changes in heart rate. Neither acute nor chronic Ang II treatment produced significant changes in plasma renin activity and norepinephrine in plasma and cerebrospinal fluid(CSF), while the plasma and CSF level of AVP was increased in the acute Ang II treatment, but not in the chronic Ang II treatment. The COR was blunted in the acute Ang II treatment compared with those obtained in the chronic Ang II or sham treatment. The blunted pressor response to carotid occlusion in the acute Ang II treatment was restored by cutting the remaining vagus nerve. These results suggest that baroreceptor reflexes are impaired by the acute excess of Ang II in the brain, and it might be mediated through increased vagal afferent activity, changes in the central integration of low and high pressure baroreceptors, and a combination of both.

Angiotensin II↗
PubMed1987

Intracellular free calcium concentration, Ca++ channel and calmodulin level in experimental hypertension in rats.

Using fluorescent calcium indicator quin2, we studied intracellular free calcium concentration in platelets that have a number of features similar to vascular smooth muscle cells. Intracellular free calcium concentration in platelets of male SHR was significantly higher at 4, 11 and 28 weeks old compared with age-matched male WKY. However, no significant difference was observed in platelets cytosolic free calcium level of DOCA-salt hypertensive and two-kidney, one clip hypertensive rats in the chronic stage. Cardiac Ca++ channels were estimated by means of radioligand binding method with [3H]-nimodipine. No significant changes were observed in the concentration and affinity of cardiac Ca++ channel in SHR, DOCA-salt hypertensive and two-kidney, one clip hypertensive rats. Calmodulin levels in mesenteric arteries of SHR were significantly decreased in comparison with those of WKY. However no significant differences were observed in DOCA-salt hypertensive rats in the chronic stage. These results indicate that the increase in intracellular free calcium concentration of SHR is not the secondary change caused by high blood pressure. It is impossible to detect the ratio of the three states (open, resting and inactivated) of Ca++ channel. Therefore, there remains a possibility of the changes in the ratio of the states of Ca++ channel. The observed abnormalities of Ca++ regulation may contribute to the pathogenesis of hypertension.

Animals↗
PubMed1987

Effects of nicardipine on blood pressure and platelet cytosolic free calcium concentration in SHR.

Intracellular free calcium concentration was measured by the fluorescent calcium indicator quin2 method in platelets of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, and the effects of nicardipine on platelet cytosolic free calcium concentration were investigated. Cytosolic free calcium concentration was significantly increased in platelets of 4-, 11-, and 14-week-old SHR compared with age-matched WKY rats. Platelet cytosolic free calcium concentration in 14-week-old male SHR was significantly decreased 1 h after the administration of nicardipine (5 mg/kg p.o.), while that in WKY rats remained unchanged. These results suggest that transmembrane Ca2+ influx is genetically increased in SHR.

Administration, Oral↗
PubMed1987

Ca mobilization from the intracellular Ca store in spontaneously hypertensive rats.

To evaluate the size of the intracellular Ca store in spontaneously hypertensive rats (SHR), caffeine-induced contractions were investigated in mesenteric artery preparation. Twelve-week-old SHR and age-matched Wistar-Kyoto (WKY) rats were used. The isolated mesenteric artery was prepared by the method of McGregor. Caffeine (2 mg)- and norepinephrine (2 micrograms)-induced pressor responses were measured in both normal (Ca, 2 mM) and Ca-free solution (1 mM EGTA solution). In the presence of Ca, pressor responses to exogenous norepinephrine in SHR were higher than those in WKY rats. In Ca-free solution, pressor responses to norepinephrine were markedly reduced in SHR compared to WKY rats and caffeine-induced contractions in SHR were lower than those in WKY rats. These results suggest that pressor responses to norepinephrine in SHR may be more dependent on extracellular Ca than in WKY rats and the caffeine-sensitive intracellular Ca store might be less in SHR.

Animals↗
PubMed1986

[The pattern of left ventricular hypertrophy in hypertension and its relation to the hemodynamic and sympathetic responses to exercise].

A wide spectrum of cardiac hypertrophy has been observed in hypertensive patients. In this study, the responses of hemodynamics and sympathetic drives to exercise among hypertensive patients with various types of left ventricular hypertrophy were investigated. Twenty-five patients with untreated essential hypertension (WHO I and II) were classified as those with and without asymmetric hypertrophy (with AH, n = 7; without AH, n = 18) by their echocardiographic patterns. Ten normotensives served as controls. Exercise was performed on a braked bicycle ergometer; the initial work load was 50 watt. The work load increased progressively by 25 watt at three minute-intervals to the target heart rate, exhaustion, or positive ST.T changes. Blood pressure, heart rate, plasma norepinephrine and hemodynamic parameters by echocardiography were estimated at rest and during exercise. Systolic blood pressure and increased heart rate by exercise in all groups. In patients with AH, a rapid increase was observed, and the increase in systolic blood pressure at submaximum exercise was significantly greater than those in normotensives or patients without AH (p less than 0.05). During exercise, endsystolic dimension decreased in normotensives and in patients without AH (p less than 0.01), but the change was not significant in patients with AH. Percent fractional shortening and percent systolic wall thickening of the interventricular septum and left ventricular posterior wall increased significantly in normotensives and in patients without AH (p less than 0.05), but they were unaltered in patients with AH. Although plasma norepinephrine significantly increased in all groups by exercise, the increase in patients with ASH was greater than those in the other groups (p less than 0.05). These results suggest that hyperresponsiveness of systolic blood pressure and heart rate to exercise may play a role in the pathogenesis of AH, and that this type of hypertrophy could be associated with abnormalities of the sympathetic nervous system.

Adult↗
PubMed1985

Plasma noradrenaline and its deaminated metabolites in essential hypertension and pheochromocytoma.

Dihydroxyphenylglycol (DOPEG) is a metabolite of noradrenaline (NA) in the sympathetic nerve endings, and dihydroxymandelic acid (DOMA) is one in the extraneuronal tissues. The measurement of plasma DOPEG and DOMA were evaluated with NA as one of the clinical indices of sympathetic nerve activity. These were measured in essential hypertension and also applied for diagnosis of pheochromocytoma. Plasma DOPEG levels were correlated with NA. Plasma NA and DOPEG were decreased after oral administration of clonidine (150 micrograms) and plasma DOPEG levels were slowly increased after standing. Therefore, plasma DOPEG seemed to be useful as one of the rather stable indices of the sympathetic nerve activity. Plasma NA and DOPEG levels in WHO stage I essential hypertension were higher than those in normotensive controls. Observed normal plasma noradrenaline and DOPEG levels in stage II reflect the normalized sympathetic tone in this stage. The elevation of plasma NA and DOMA levels in stage III seemed to be at least partly explained by renal function disturbance. In patients with pheochromocytoma, despite of the marked elevation of plasma NA and DOMA, plasma DOPEG showed only three-fold elevation and the ratio DOPEG/NA was reduced. The simultaneous measurement of plasma NA, DOPEG and DOMA is useful to evaluate sympathetic nerve activity in essential hypertension and to differentiate pheochromocytoma in hypertension.

Adrenal Gland Neoplasms↗
PubMed1984

Neurotransmitter release and vascular reactivity in spontaneously hypertensive rats.

This study was designed to investigate neurotransmitter release during the sympathetic nerve stimulation of perfused mesenteric arterial beds of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) at young and adult ages. The role of Ca in neurotransmitter release and vascular responsiveness was also examined by using a Ca-antagonist (verapamil). Pressor responses to electrical nerve stimulation and exogenous noradrenaline were greater in SHR than in WKY. Noradrenaline overflow by electrical nerve stimulation from mesenteric arterial beds was also significantly greater in young SHR than age-matched WKY. However, in adult SHR, the noradrenaline overflow was reduced compared with WKY. After verapamil infusion (5.0 X 10(-7)M approximately 2.5 X 10(-6)M), suppression of the pressor responses and noradrenaline overflow evoked by electrical nerve stimulation was greater in SHR than in WKY at both ages. The pressor responses to exogenous noradrenaline were also inhibited by verapamil more in young SHR than in young WKY. In adult SHR, the inhibition was similar to age-matched WKY. These results suggest that noradrenaline release from sympathetic nerve endings in SHR increase at a young age and decreases in adults, and depends at least partly on Ca-influx at both ages as dose vasoconstrictor reactivity. Therefore, Ca-dependency in SHR at both pre- and post-synaptic sites of neurotransmission may contribute to the pathogenesis of hypertension.

Animals↗
PubMed1984

Alteration of presynaptic alpha 2-mediated inhibition of norepinephrine release in perfused mesenteric arteries of young and adult spontaneously hypertensive rats.

The present study was designed to evaluate norepinephrine release during sympathetic nerve stimulation and its inhibitory characteristics by presynaptic alpha 2-adrenoceptor in the perfused mesenteric arteries of young and old spontaneously hypertensive rats (SHR) compared with age-matched Wistar-Kyoto rats (WKY). Sympathetic nerve stimulation caused significantly greater overflow of endogenous norepinephrine from adrenergic nerve terminals in young SHR than age-matched WKY. Yohimbine, alpha 2-adrenoceptor antagonist, exerted a facilitatory effect on norepinephrine overflow from mesenteric vasculature. This effect was less in young SHR than in aged-matched WKY. On the other hand, in adult SHR the amount of norepinephrine overflow was somewhat reduced compared with age-matched WKY. The difference of the facilitatory effect on norepinephrine overflow by yohimbine between SHR and WKY was not so marked as that observed in young age. These results indicate that increased norepinephrine release from sympathetic nerve endings in young SHR could depend at least partly on impaired presynaptic alpha 2-mediated inhibition, while normal or reduced norepinephrine release in adult SHR might be an adaptive mechanism to prevent further increase in blood pressure in SHR.

Aging↗
PubMed1984

Neurotransmitter release, vascular responsiveness and their calcium-mediated regulation in perfused mesenteric preparation of spontaneously hypertensive rats and DOCA-salt hypertension.

To investigate the role of norepinephrine release from the sympathetic nerve endings and vascular responsiveness to endogenous and exogenous norepinephrine in the pathogenesis of hypertension, the perfused mesenteric preparations from spontaneously hypertensive rats (SHR) and DOCA-salt hypertension were used. In addition, the effects of two calcium antagonists on norepinephrine release by electrical stimulation and the vasoconstrictor responses to norepinephrine were examined to evaluate the calcium dependency of norepinephrine release and the vascular responsiveness in hypertension. The vascular responsiveness was increased in SHR and DOCA-salt hypertension in both early and later phases. Norepinephrine overflow from the sympathetic nerve terminals was enhanced only in young SHR and the chronic phase of DOCA-salt hypertension. After infusion of verapamil, a calcium antagonist, into the perfusate, the pressor responses and norepinephrine overflow by electrical stimulation were more inhibited in SHR, especially in young SHR, and the chronic phase of DOCA-salt hypertension than in controls. These results suggest that calcium dependency in both pre- and postsynaptic sites of neurotransmission may contribute to the pathogenesis of hypertension.

Animals↗
PubMed1983

Changes in renal alpha 2-adrenoceptor in experimental hypertension in rats.

alpha 2-Adrenoceptors were studied in renal membrane fractions from spontaneously hypertensive (SHR), two-kidney, one clip hypertensive (2K, 1C HT) and DOCA-salt hypertensive (DOCA-salt HT) rats, using radioligand binding method. alpha 2-Adrenoceptor concentration in the kidney measured by [3H]yohimbine binding was significantly increased in SHR at 4 weeks old (41.5 +/- 2.8 fmol/mg protein, mean +/- SEM, p less than 0.01), 12 weeks old (54.9 +/- 2.5 fmol/mg protein, p less than 0.01) and 35 weeks old (59.8 +/- 3.4 fmol/mg protein, p less than 0.01) as compared with age-matched Wistar-Kyoto rats (WKY, 31.5 +/- 2.5, 40.9 +/- 1.8, 47.8 +/- 2.0 fmol/mg protein, respectively). There were no significant differences in binding affinity and 5'-nucleotidase activity (plasma membrane marker enzyme) between SHR and WKY at any age. In 2K, 1C HT rats, alpha 2-adrenoceptor concentration in the clipped kidney was higher than that of control rats, but alpha 2-adrenoceptor concentration in the unclipped kidney was unchanged. Binding affinity and 5'-nucleotidase activity showed no significant changes in renal hypertensive rats. In DOCA-salt HT rats, no significant change was found in concentration and affinity of renal alpha 2-adrenoceptor. The observed increase in renal alpha 2-adrenoceptor concentration in SHR may contribute to the pathogenesis and maintenance of hypertension through increased sodium and water reabsorption in the kidney.

Animals↗
PubMed1981

Changes in cardiac beta-adrenoceptor concentrations in spontaneously hypertensive and experimental renal hypertensive rats.

Cardiac beta-adrenoceptors were studied in membrane fractions from spontaneously hypertensive rats (SHR) and rats with two-kidney, one clip hypertension (2K, 1C HT), using radioligand binding method. beta-Adrenoceptor concentration measured by [3H]-dihydroalprenolol (DHA) binding was significantly lower in cardiac membranes from two months old SHR than those from Wistar-Kyoto rats (WKY) (38.2 +/- 2.6 vs 45.1 +/- 1.8 fmol/mg protein, means +/- SEM, p less than 0.05). Cardiac membranes from 2K, 1C HT rats had also a lower concentration of beta-adrenoceptors than those from the sham-operated control rats at a week after operation (30.9 +/- 2.2 vs 47.8 +/- 1.6 fmol/mg protein, p less than 0.01). But receptor affinity remained unchanged. These reduced concentrations of beta-adrenoceptors were restored to control levels at 12 months old in SHR and at 6 weeks after operation in 2K, 1C HT rats, although age-dependent decrease in beta-adrenoceptor was observed. The decrease in beta-adrenoceptor was associated with increase in plasma noradrenaline levels during the earlier stages of hypertension. But there is no correlation between beta-adrenoceptor concentrations and plasma noradrenaline levels in the chronic stages of hypertension. No significant difference was found in activities of 5'-nucleotidase, which is a marker enzyme of cell membrane, in membrane fractions between the hypertensive hearts and the controls, suggesting that the cardiac hypertrophy is not a determinant factor for change in beta-adrenoceptor. The observed decrease in beta-adrenoceptor concentration may reflect an increase in sympathetic nerve activity during development of hypertension. In the chronic stages of hypertension, additional factors may be involved in the restoration of beta-adrenoceptors.

5'-Nucleotidase↗